The frequency of a pronounced hypertrophy of the heart in kidney disease was first pointed out by Bright1 in 1836. It was exhibited in 23 per cent. of his cases, in most of them affecting the left ventricle, without any cardiac or aortic lesion as a cause. His theory, chemical in nature, considered that an altered condition of the blood either stimulated the heart excessively or else affected the arteries and capillaries in some way to make it more difficult for the heart to drive the blood through to the veins.

G. Johnson2 confirmed his findings and adopted the second possibility as an explanation, assuming that the blood is laden with impurities as a result of the renal disease, and that these poisons stimulate the arterioles to contract by way of the vasomotor nerves and so necessitate an hypertrophy of the left ventricle. His conception assumed the existence